Emodin Induces Apoptosis of Human Tongue Squamous Cancer SCC-4 Cells through Reactive Oxygen Species and Mitochondria-dependent Pathways
Emodin was isolated from Rheum palmatum L. and exhibits an anticancer effect on human cancer cell lines, however, the molecular mechanisms of emodin-mediated apoptosis in human tongue cancer cells have not been fully investigated. In this study, treatment of human tongue cancer SCC-4 cells with vari...
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| Veröffentlicht in: | Anticancer research 2009-01, Vol.29 (1), p.327-335 |
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| creator | LIN, Shuw-Yuan LAI, Wan-Wen CHUNG, Jing-Gung HO, Chin-Chin YU, Fu-Shun CHEN, Guang-Wei YANG, Jai-Sing LIU, Kuo-Ching LIN, Meng-Liang WU, Ping-Ping FAN, Ming-Jen |
| description | Emodin was isolated from Rheum palmatum L. and exhibits an anticancer effect on human cancer cell lines, however, the molecular
mechanisms of emodin-mediated apoptosis in human tongue cancer cells have not been fully investigated. In this study, treatment
of human tongue cancer SCC-4 cells with various concentrations of emodin led to G 2 /M arrest through promoted p21 and Chk2 expression but inhibited cyclin B1 and cdc2; it also induced apoptosis through the
pronounced release of cytochrome c from mitochondria and activations of caspase-9 and caspase-3. These events were accompanied
by the generation of reactive oxygen species (ROS), disruption of mitochondrial membrane potential (ÎΨ m ) and a decrease in the ratio of mitochondrial Bcl-2 and Bax content; emodin also promoted the levels of GADD153 and GRP78.
The free radical scavenger N-acetylcysteine and caspase inhibitors markedly blocked emodin-induced apoptosis. Taken together,
these findings suggest that emodin mediated oxidative injury (DNA damage) based on ROS production and ER stress based on the
levels of GADD153 and GRP78 that acts as an early and upstream change in the cell death cascade to caspase- and mitochondria-dependent
signaling pathways, triggers mitochondrial dysfunction from Bcl-2 and Bax modulation, mitochondrial cytochrome c release and
caspase activation, consequently leading to apoptosis in SCC-4 cells. |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_proquest_miscellaneous_67094817</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>67094817</sourcerecordid><originalsourceid>FETCH-LOGICAL-h198t-6435a49c8a0fe2e0d0be7c74e9eddc1965eb4a65ea9c96b4c077ab7be858a063</originalsourceid><addsrcrecordid>eNo90M1O6zAQBeAIXQTl5xWQF1x2kew4ieMliuCCBALR7qOJPW2MEjvYCb19Ax4bCwqbmc03R5pzkCyYkCwVBad_kgXNCpoKSovj5CSEV0rLUlb8KDlmknPGSrlIPm4Gp40l91bPCgO5Ht04uWACcWtyNw9gycrZzYxk-TbD4OZAarAKPVnWdZqTGvs-kKnzbt505AVBTeYdydP_3QYtWY6oTEwFq8mjmZzqnNXeQKpxRKvRTuQZpm4Lu3CWHK6hD3i-36fJ6vZmVd-lD0__7uvrh7RjsprSMucF5FJVQNeYIdW0RaFEjhK1VkyWBbY5xAlSybLNFRUCWtFiVcSTkp8mV9-xo3dvM4apGUxQ8QmwGJ9rSkFlXjER4cUezu2Auhm9GcDvmp_qIvi7BxAU9GsfazHh12XsS-bRXX67zmy6rfHYhAH6PsbyBnwmG9bwTPBPH6WHFA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>67094817</pqid></control><display><type>article</type><title>Emodin Induces Apoptosis of Human Tongue Squamous Cancer SCC-4 Cells through Reactive Oxygen Species and Mitochondria-dependent Pathways</title><source>MEDLINE</source><source>EZB-FREE-00999 freely available EZB journals</source><creator>LIN, Shuw-Yuan ; LAI, Wan-Wen ; CHUNG, Jing-Gung ; HO, Chin-Chin ; YU, Fu-Shun ; CHEN, Guang-Wei ; YANG, Jai-Sing ; LIU, Kuo-Ching ; LIN, Meng-Liang ; WU, Ping-Ping ; FAN, Ming-Jen</creator><creatorcontrib>LIN, Shuw-Yuan ; LAI, Wan-Wen ; CHUNG, Jing-Gung ; HO, Chin-Chin ; YU, Fu-Shun ; CHEN, Guang-Wei ; YANG, Jai-Sing ; LIU, Kuo-Ching ; LIN, Meng-Liang ; WU, Ping-Ping ; FAN, Ming-Jen</creatorcontrib><description>Emodin was isolated from Rheum palmatum L. and exhibits an anticancer effect on human cancer cell lines, however, the molecular
mechanisms of emodin-mediated apoptosis in human tongue cancer cells have not been fully investigated. In this study, treatment
of human tongue cancer SCC-4 cells with various concentrations of emodin led to G 2 /M arrest through promoted p21 and Chk2 expression but inhibited cyclin B1 and cdc2; it also induced apoptosis through the
pronounced release of cytochrome c from mitochondria and activations of caspase-9 and caspase-3. These events were accompanied
by the generation of reactive oxygen species (ROS), disruption of mitochondrial membrane potential (ÎΨ m ) and a decrease in the ratio of mitochondrial Bcl-2 and Bax content; emodin also promoted the levels of GADD153 and GRP78.
The free radical scavenger N-acetylcysteine and caspase inhibitors markedly blocked emodin-induced apoptosis. Taken together,
these findings suggest that emodin mediated oxidative injury (DNA damage) based on ROS production and ER stress based on the
levels of GADD153 and GRP78 that acts as an early and upstream change in the cell death cascade to caspase- and mitochondria-dependent
signaling pathways, triggers mitochondrial dysfunction from Bcl-2 and Bax modulation, mitochondrial cytochrome c release and
caspase activation, consequently leading to apoptosis in SCC-4 cells.</description><identifier>ISSN: 0250-7005</identifier><identifier>EISSN: 1791-7530</identifier><identifier>PMID: 19331169</identifier><language>eng</language><publisher>Attiki: International Institute of Anticancer Research</publisher><subject>Apoptosis - drug effects ; Apoptosis - physiology ; Biological and medical sciences ; Calcium - metabolism ; Carcinoma, Squamous Cell - drug therapy ; Carcinoma, Squamous Cell - metabolism ; Carcinoma, Squamous Cell - pathology ; Caspase 3 - metabolism ; Caspase 9 - metabolism ; CDC2 Protein Kinase ; Cell Division - drug effects ; Checkpoint Kinase 2 ; Cyclin B - antagonists & inhibitors ; Cyclin B1 ; Cyclin-Dependent Kinase Inhibitor p21 - biosynthesis ; Cyclin-Dependent Kinases ; DNA Damage ; Emodin - pharmacology ; G2 Phase - drug effects ; Humans ; Medical sciences ; Membrane Potential, Mitochondrial - drug effects ; Mitochondria - drug effects ; Mitochondria - physiology ; Otorhinolaryngology. Stomatology ; Protein-Serine-Threonine Kinases - biosynthesis ; Reactive Oxygen Species - metabolism ; Tongue Neoplasms - drug therapy ; Tongue Neoplasms - metabolism ; Tongue Neoplasms - pathology ; Tumors ; Upper respiratory tract, upper alimentary tract, paranasal sinuses, salivary glands: diseases, semeiology</subject><ispartof>Anticancer research, 2009-01, Vol.29 (1), p.327-335</ispartof><rights>2009 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,4010</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21193314$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19331169$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>LIN, Shuw-Yuan</creatorcontrib><creatorcontrib>LAI, Wan-Wen</creatorcontrib><creatorcontrib>CHUNG, Jing-Gung</creatorcontrib><creatorcontrib>HO, Chin-Chin</creatorcontrib><creatorcontrib>YU, Fu-Shun</creatorcontrib><creatorcontrib>CHEN, Guang-Wei</creatorcontrib><creatorcontrib>YANG, Jai-Sing</creatorcontrib><creatorcontrib>LIU, Kuo-Ching</creatorcontrib><creatorcontrib>LIN, Meng-Liang</creatorcontrib><creatorcontrib>WU, Ping-Ping</creatorcontrib><creatorcontrib>FAN, Ming-Jen</creatorcontrib><title>Emodin Induces Apoptosis of Human Tongue Squamous Cancer SCC-4 Cells through Reactive Oxygen Species and Mitochondria-dependent Pathways</title><title>Anticancer research</title><addtitle>Anticancer Res</addtitle><description>Emodin was isolated from Rheum palmatum L. and exhibits an anticancer effect on human cancer cell lines, however, the molecular
mechanisms of emodin-mediated apoptosis in human tongue cancer cells have not been fully investigated. In this study, treatment
of human tongue cancer SCC-4 cells with various concentrations of emodin led to G 2 /M arrest through promoted p21 and Chk2 expression but inhibited cyclin B1 and cdc2; it also induced apoptosis through the
pronounced release of cytochrome c from mitochondria and activations of caspase-9 and caspase-3. These events were accompanied
by the generation of reactive oxygen species (ROS), disruption of mitochondrial membrane potential (ÎΨ m ) and a decrease in the ratio of mitochondrial Bcl-2 and Bax content; emodin also promoted the levels of GADD153 and GRP78.
The free radical scavenger N-acetylcysteine and caspase inhibitors markedly blocked emodin-induced apoptosis. Taken together,
these findings suggest that emodin mediated oxidative injury (DNA damage) based on ROS production and ER stress based on the
levels of GADD153 and GRP78 that acts as an early and upstream change in the cell death cascade to caspase- and mitochondria-dependent
signaling pathways, triggers mitochondrial dysfunction from Bcl-2 and Bax modulation, mitochondrial cytochrome c release and
caspase activation, consequently leading to apoptosis in SCC-4 cells.</description><subject>Apoptosis - drug effects</subject><subject>Apoptosis - physiology</subject><subject>Biological and medical sciences</subject><subject>Calcium - metabolism</subject><subject>Carcinoma, Squamous Cell - drug therapy</subject><subject>Carcinoma, Squamous Cell - metabolism</subject><subject>Carcinoma, Squamous Cell - pathology</subject><subject>Caspase 3 - metabolism</subject><subject>Caspase 9 - metabolism</subject><subject>CDC2 Protein Kinase</subject><subject>Cell Division - drug effects</subject><subject>Checkpoint Kinase 2</subject><subject>Cyclin B - antagonists & inhibitors</subject><subject>Cyclin B1</subject><subject>Cyclin-Dependent Kinase Inhibitor p21 - biosynthesis</subject><subject>Cyclin-Dependent Kinases</subject><subject>DNA Damage</subject><subject>Emodin - pharmacology</subject><subject>G2 Phase - drug effects</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Membrane Potential, Mitochondrial - drug effects</subject><subject>Mitochondria - drug effects</subject><subject>Mitochondria - physiology</subject><subject>Otorhinolaryngology. Stomatology</subject><subject>Protein-Serine-Threonine Kinases - biosynthesis</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Tongue Neoplasms - drug therapy</subject><subject>Tongue Neoplasms - metabolism</subject><subject>Tongue Neoplasms - pathology</subject><subject>Tumors</subject><subject>Upper respiratory tract, upper alimentary tract, paranasal sinuses, salivary glands: diseases, semeiology</subject><issn>0250-7005</issn><issn>1791-7530</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo90M1O6zAQBeAIXQTl5xWQF1x2kew4ieMliuCCBALR7qOJPW2MEjvYCb19Ax4bCwqbmc03R5pzkCyYkCwVBad_kgXNCpoKSovj5CSEV0rLUlb8KDlmknPGSrlIPm4Gp40l91bPCgO5Ht04uWACcWtyNw9gycrZzYxk-TbD4OZAarAKPVnWdZqTGvs-kKnzbt505AVBTeYdydP_3QYtWY6oTEwFq8mjmZzqnNXeQKpxRKvRTuQZpm4Lu3CWHK6hD3i-36fJ6vZmVd-lD0__7uvrh7RjsprSMucF5FJVQNeYIdW0RaFEjhK1VkyWBbY5xAlSybLNFRUCWtFiVcSTkp8mV9-xo3dvM4apGUxQ8QmwGJ9rSkFlXjER4cUezu2Auhm9GcDvmp_qIvi7BxAU9GsfazHh12XsS-bRXX67zmy6rfHYhAH6PsbyBnwmG9bwTPBPH6WHFA</recordid><startdate>20090101</startdate><enddate>20090101</enddate><creator>LIN, Shuw-Yuan</creator><creator>LAI, Wan-Wen</creator><creator>CHUNG, Jing-Gung</creator><creator>HO, Chin-Chin</creator><creator>YU, Fu-Shun</creator><creator>CHEN, Guang-Wei</creator><creator>YANG, Jai-Sing</creator><creator>LIU, Kuo-Ching</creator><creator>LIN, Meng-Liang</creator><creator>WU, Ping-Ping</creator><creator>FAN, Ming-Jen</creator><general>International Institute of Anticancer Research</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>20090101</creationdate><title>Emodin Induces Apoptosis of Human Tongue Squamous Cancer SCC-4 Cells through Reactive Oxygen Species and Mitochondria-dependent Pathways</title><author>LIN, Shuw-Yuan ; LAI, Wan-Wen ; CHUNG, Jing-Gung ; HO, Chin-Chin ; YU, Fu-Shun ; CHEN, Guang-Wei ; YANG, Jai-Sing ; LIU, Kuo-Ching ; LIN, Meng-Liang ; WU, Ping-Ping ; FAN, Ming-Jen</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h198t-6435a49c8a0fe2e0d0be7c74e9eddc1965eb4a65ea9c96b4c077ab7be858a063</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Apoptosis - drug effects</topic><topic>Apoptosis - physiology</topic><topic>Biological and medical sciences</topic><topic>Calcium - metabolism</topic><topic>Carcinoma, Squamous Cell - drug therapy</topic><topic>Carcinoma, Squamous Cell - metabolism</topic><topic>Carcinoma, Squamous Cell - pathology</topic><topic>Caspase 3 - metabolism</topic><topic>Caspase 9 - metabolism</topic><topic>CDC2 Protein Kinase</topic><topic>Cell Division - drug effects</topic><topic>Checkpoint Kinase 2</topic><topic>Cyclin B - antagonists & inhibitors</topic><topic>Cyclin B1</topic><topic>Cyclin-Dependent Kinase Inhibitor p21 - biosynthesis</topic><topic>Cyclin-Dependent Kinases</topic><topic>DNA Damage</topic><topic>Emodin - pharmacology</topic><topic>G2 Phase - drug effects</topic><topic>Humans</topic><topic>Medical sciences</topic><topic>Membrane Potential, Mitochondrial - drug effects</topic><topic>Mitochondria - drug effects</topic><topic>Mitochondria - physiology</topic><topic>Otorhinolaryngology. Stomatology</topic><topic>Protein-Serine-Threonine Kinases - biosynthesis</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Tongue Neoplasms - drug therapy</topic><topic>Tongue Neoplasms - metabolism</topic><topic>Tongue Neoplasms - pathology</topic><topic>Tumors</topic><topic>Upper respiratory tract, upper alimentary tract, paranasal sinuses, salivary glands: diseases, semeiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>LIN, Shuw-Yuan</creatorcontrib><creatorcontrib>LAI, Wan-Wen</creatorcontrib><creatorcontrib>CHUNG, Jing-Gung</creatorcontrib><creatorcontrib>HO, Chin-Chin</creatorcontrib><creatorcontrib>YU, Fu-Shun</creatorcontrib><creatorcontrib>CHEN, Guang-Wei</creatorcontrib><creatorcontrib>YANG, Jai-Sing</creatorcontrib><creatorcontrib>LIU, Kuo-Ching</creatorcontrib><creatorcontrib>LIN, Meng-Liang</creatorcontrib><creatorcontrib>WU, Ping-Ping</creatorcontrib><creatorcontrib>FAN, Ming-Jen</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Anticancer research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>LIN, Shuw-Yuan</au><au>LAI, Wan-Wen</au><au>CHUNG, Jing-Gung</au><au>HO, Chin-Chin</au><au>YU, Fu-Shun</au><au>CHEN, Guang-Wei</au><au>YANG, Jai-Sing</au><au>LIU, Kuo-Ching</au><au>LIN, Meng-Liang</au><au>WU, Ping-Ping</au><au>FAN, Ming-Jen</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Emodin Induces Apoptosis of Human Tongue Squamous Cancer SCC-4 Cells through Reactive Oxygen Species and Mitochondria-dependent Pathways</atitle><jtitle>Anticancer research</jtitle><addtitle>Anticancer Res</addtitle><date>2009-01-01</date><risdate>2009</risdate><volume>29</volume><issue>1</issue><spage>327</spage><epage>335</epage><pages>327-335</pages><issn>0250-7005</issn><eissn>1791-7530</eissn><abstract>Emodin was isolated from Rheum palmatum L. and exhibits an anticancer effect on human cancer cell lines, however, the molecular
mechanisms of emodin-mediated apoptosis in human tongue cancer cells have not been fully investigated. In this study, treatment
of human tongue cancer SCC-4 cells with various concentrations of emodin led to G 2 /M arrest through promoted p21 and Chk2 expression but inhibited cyclin B1 and cdc2; it also induced apoptosis through the
pronounced release of cytochrome c from mitochondria and activations of caspase-9 and caspase-3. These events were accompanied
by the generation of reactive oxygen species (ROS), disruption of mitochondrial membrane potential (ÎΨ m ) and a decrease in the ratio of mitochondrial Bcl-2 and Bax content; emodin also promoted the levels of GADD153 and GRP78.
The free radical scavenger N-acetylcysteine and caspase inhibitors markedly blocked emodin-induced apoptosis. Taken together,
these findings suggest that emodin mediated oxidative injury (DNA damage) based on ROS production and ER stress based on the
levels of GADD153 and GRP78 that acts as an early and upstream change in the cell death cascade to caspase- and mitochondria-dependent
signaling pathways, triggers mitochondrial dysfunction from Bcl-2 and Bax modulation, mitochondrial cytochrome c release and
caspase activation, consequently leading to apoptosis in SCC-4 cells.</abstract><cop>Attiki</cop><pub>International Institute of Anticancer Research</pub><pmid>19331169</pmid><tpages>9</tpages></addata></record> |
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| subjects | Apoptosis - drug effects Apoptosis - physiology Biological and medical sciences Calcium - metabolism Carcinoma, Squamous Cell - drug therapy Carcinoma, Squamous Cell - metabolism Carcinoma, Squamous Cell - pathology Caspase 3 - metabolism Caspase 9 - metabolism CDC2 Protein Kinase Cell Division - drug effects Checkpoint Kinase 2 Cyclin B - antagonists & inhibitors Cyclin B1 Cyclin-Dependent Kinase Inhibitor p21 - biosynthesis Cyclin-Dependent Kinases DNA Damage Emodin - pharmacology G2 Phase - drug effects Humans Medical sciences Membrane Potential, Mitochondrial - drug effects Mitochondria - drug effects Mitochondria - physiology Otorhinolaryngology. Stomatology Protein-Serine-Threonine Kinases - biosynthesis Reactive Oxygen Species - metabolism Tongue Neoplasms - drug therapy Tongue Neoplasms - metabolism Tongue Neoplasms - pathology Tumors Upper respiratory tract, upper alimentary tract, paranasal sinuses, salivary glands: diseases, semeiology |
| title | Emodin Induces Apoptosis of Human Tongue Squamous Cancer SCC-4 Cells through Reactive Oxygen Species and Mitochondria-dependent Pathways |
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